R. Okeda et al., STUDY ON THE ETIOPATHOGENESIS OF MULTIPLE SPONGY NECROSIS OF THE PONTINE BASE IN 3 AUTOPSY CASES, Acta Neuropathologica, 96(2), 1998, pp. 123-128
The etiopathogenesis of multiple spongv necrosis (MSN) of the pontine
base was analyzed by examining the spatial relationship with intra- an
d extrafascicular vascular structures by reconstruction of serial sect
ions of nine lesions from three autopsy cases. All nine lesions in the
fascicles were distributed without any spatial relationship to the in
trafascicular vessels. Instead, these lesions were distributed in para
llel with arterial and venous transverse main branches between the ant
eromedial and anterolateral groups of the pontine vessels. On the othe
r hand, all lesions in the middle cerebellar peduncle were arranged ob
liquely along the arterial and venous main trunks of the lateral group
vessels with sparing of the perivascular narrow zone of the white mat
ter. Moreover, narrow fascicles, even though located in the dorsomedia
l region of the pontine base, which is consistently involved in MSN, w
ere spared, and thick transverse and longitudinal fascicles were selec
tively involved. The marginal zone of fascicles was spaced, and focal
coagulation necrosis was sometimes found in MSN lesions. Additionally,
normal fascicles did not have their own nutritional arteries, and wer
e nourished by arterioles and capillaries from the surrounding pontine
gray matter. Neither severe organic stenosis nor occlusion of pontine
vessels was found. On the basis of the close topographical relationsh
ip of MSN lesions with the pontine vascular architecture in addition t
o preferential involvement of thick fascicles with sparing of the marg
inal zone and inclusion of focal coagulation necrosis, it is proposed
that the etiopathogenesis of MSN is pontine ischemia on a background o
f the characteristic parenchymal and vascular architecture of the pont
ine base. As to the cause of the ischemia, it is proposed that some fu
nctional disorder such as arterial vasoconstriction in the pontine bas
e or the vertebrobasilar artery is responsible, rather than organic ch
anges in the vessles.